View Full Version : Aspartame + MSM...
August 19th, 2003, 06:33 AM
Ok, I have done some research concerning aspartame as an additive in foods and although many commercial site claim it is BAD with a capita B, there is no real evidence to support this...marketing gimmick, perhaps? and yes, it was approved by the FDA (they would have you believe they are adding this "poison" to our food as some kind of conspiracy theory). I even went to JAMA and they say that it is not recommended for diabetics, but for others normal consumption is perfectly safe.
As far as MSM, it's the same scenario...no real proof and most research I did find describe the benefits of MSM and how forms of it are found in natural fruits like fruits and veggies and this is even administered to elderly patients at healthcare facilities where my husband works. If it was toxic, imagine the lawsuits waiting to happen.
Anyway, if someone knows of a scientific site that has more info on adverse effects of either, please let me know...still in the market to learn more about what I am consuming and I know you ladies are very knowledgeable.
August 19th, 2003, 09:06 AM
Let me research this for you. I haven't heard anything bad about MSM, this is the first I've heard of this.
HOWEVER, I did had several aspartame sites sent to me by my MIL, DH drinks diet pop by the gallon, quite literally and she sent me stuff about studies that show it damages brain cells, etc etc. I have never touched it, just didn't like the taste and wouldn't touch it for a million bucks now.
Let me see if she's still got them, I"ve switched computers since then and dont' have them at hand.
August 19th, 2003, 09:36 AM
Here's what a search brought up for me - use it to form your own opinion, lol ... I haven't had enough time to read it all.
Source: NEUROLOGY; 43 (3 PART 1). 1993. 611-613.
BIOSIS COPYRIGHT: BIOL ABS. The artificial sweetener aspartame (NutraSweet) is hydrolyzed in the gut as phenylalanine (PA), a large neutral amino acid (LNAA). LNAAs compete with levodopa for uptake into the brain. To determine the effect of aspartame on levodopa-treated Parkinson's disease (PD) patients, we studied 18 PD patients with protein-sensitive motor fluctuations by administering in a double-blind and single-crossover design, on alternate days, aspartame (600 or 1,200 mg) and placebo.
Every hour, we performed a motor examination and drew blood to estimate plasma LNAA, PA, and levodopa levels. Six-hundred mg of aspartame had no effect on plasma PA or motor status. Although 1,200 mg of aspartame significantly increased plasma PA, motor performance did not deteriorate. Aspartame consumption in amounts well in excess of what would be consumed by heavy users of aspartame-sweetened products has no adverse effect on PD patients.
Source: Arch. Intern. Med.; VOL 149 ISS Oct 1989, P2318-2324, (REF 40)
IPA COPYRIGHT: ASHP A double-blind, placebo-controlled study of the safety of aspartame (NutraSweet; I) was conducted in 108 volunteers, aged 18-62 yr, 53 of whom were given I at a dose of 75 mg/kg for 24 wk. No persistent changes over time were noted in either group in vital signs; body weight; results of standard laboratory tests; fasting blood levels of the constituent amino acids of I, other amino acids, and methanol; or blood formate levels and 24 h urinary excretion of formate.
There also were no significant differences between groups in the number of subjects experiencing symptoms or in the number of symptoms per subject. It was concluded that these results further document the safety of the long term consumption of I at doses equivalent to the amount of I in approximately 10 liters of beverage per day.
Source: Hosp. Formul.; VOL 23 ISS Jun 1988, P543-546, (REF 19)
IPA COPYRIGHT: ASHP A review of reports of side effects attributed to the sweetening agent aspartame (NutraSweet; Equal; I) is presented. It was concluded that individuals who consume less than 50 mg/kg/day of I should not experience any adverse effects.
Source: Clin. Pharmacol. Ther.; VOL 63 ISS May 1998, P580-593, (REF 34)
IPA COPYRIGHT: ASHP The potential use of aspartame in the treatment of osteoarthritis was investigated in 2 clinical pharmacologic studies, the effect of aspartame on bleeding times in 34 normal volunteers was assessed in a double blind, placebo controlled, randomized, parallel group study, and the antipyretic effect of this agent was studied after the administration of a gavage of aspartame in Sprague-Dawley rats with turpentine-induced fever. In the first pharmacologic study, the analgesic effect and effect on performance of aspartame was assessed in a placebo controlled study conducted in 1 patient with osteoarthritis who received oral tablets of aspartame.
In the second pharmacologic study, the same effects were assessed in a double blind, placebo controlled, randomized, crossover study conducted in 13 patients with osteoarthritis who received 4 or 8 oral tablets of 19 mg of aspartame (Equal). The results showed that aspartame is biologically active. It relieved pain and improved performance in patients with osteoarthritis and induced mild antithrombotic effects. It also decreased fever in rats.
Saudi Pharm. J.; VOL 4 ISS 3-4 1996, P149-156, (REF 33)
IPA COPYRIGHT: ASHP The effect of aspartame on seizure susceptibility and its possible influence on the anticonvulsant action of ethosuximide, valproate sodium, and phenytoin sodium in mice was investigated. Aspartame, when given as a single 1 g/kg oral dose or repeated oral doses of 100 mg/kg for 14 days, neither affected the spontaneous locomotor activity of mice in an open field nor altered pentylenetetrazol (PTZ)-induced seizure threshold.
Subacute, but not acute, aspartame administration was found to decrease the anticonvulsant activity of ethosuximide and valproate in PTZ-induced seizure threshold, and of phenytoin in PTZ-induced generalized tonic clonic seizures. The antagonism of the anticonvulsant activity of ethosuximide, valproate, and phenytoin was not due to alterations of plasma levels or pharmacokinetics of the antiepileptic drugs, but could be due to an increase of brain excitatory and/or decrease of brain inhibitory neurotransmitters.
It was concluded that repeated oral low dose aspartame administration may antagonize the anticonvulsant activity of ethosuximide, valproate, and phenytoin.
J. NUTR. 1983, 113(9) 1851-1860
EIS: Epidemiology Information System ASPARTAME IS A DIPEPTIDE SWEETENER CONTAINING ASPARTATE. IT HAS BEEN SUGGESTED THAT ASPARTAME ADDITION TO MEALS CONTAINING LARGE AMOUNTS OF MONOSODIUM L-GLUTAMATE (MSG) WOULD RESULT IN A RAPID RISE IN PLASMA GLUTAMATE AND ASPARTATE CONCENTRATIONS AND INCREASE THE POTENTIAL FOR DICARBOXYLIC AMINO ACID-INDUCED TOXICITY.
SIX NORMAL ADULT SUBJECTS WERE FED THREE HAMBURGER AND MILK SHAKE MEALS PROVIDING PROTEIN AT 1 G/KG BODY WEIGHT IN A LATIN SQUARE DESIGN. ONE MEAL HAD NO ADDITIONS, THE SECOND PROVIDED MSG AT 150 MG/KG BODY WEIGHT, AND THE THIRD PROVIDED MSG AT 150 MG/KG BODY WEIGHT AND ASPARTAME AT 23 MG/KG BODY WEIGHT. THE ADDITION OF MSG ALONE SIGNIFICANTLY INCREASED PLASMA GLUTAMATE + ASPARTATE CONCENTRATION ABOVE VALUES NOTED AFTER INGESTION OF THE MEAL ALONE.
ASPARTAME ADDITION TO MEALS ALREADY CONTAINING MSG DID NOT FURTHER SIGNIFICANTLY INCREASE PLASMA GLUTAMATE + ASPARTATE CONCENTRATION ABOVE VALUES NOTED WHEN ONLY MSG WAS ADDED. HOWEVER, ASPARTAME ADDITION DID SIGNIFICANTLY INCREASE THE MEAN PLASMA PHENYLALANINE CONCENTRATION ABOVE VALUES NOTED AFTER INGESTION OF THE MEAL ALONE OR THE MEAL WITH ADDED MSG, REFLECTING ASPARTAME'S PHENYLALANINE CONTENT.
THE DATA DO NOT SUPPORT THE SUGGESTION THAT ASPARTAME ADDITION TO HIGH PROTEIN MEALS ALREADY CONTAINING LARGE AMOUNTS OF MSG, WILL PROMOTE A RAPID AND DANGEROUS RISE IN PLASMA GLUTAMATE AND ASPARTATE CONCENTRATIONS./CEREBROSPINAL FLUID
(my sincere apologies for the caps in that one... why the heck can't they type their abstracts normally???)
AM J CLIN NUTR; 34 (9). 1981. 1899-1905.
HEEP COPYRIGHT: BIOL ABS. It has been postulated that individuals (human) reporting an idiosyncratic symptom after glutamate ingestion (Chinese Restaurant Syndrome) might also experience such symptosm after aspartame (L-aspartyl-L-phenyl alanyl methyl ester) ingestion. Such sensitive subjects might have been missed in earlier studies of aspartame. Six subjects reporting various symptoms after glutamate ingestion, but not after placebo, were administered aspartame (34 mg/kg body weight) or sucrose (1 g/kg body weight) dissolved in orange juice in a randomized, cross-over, double-blind study.
No subject reported symptoms typical of glutamate response after either sucrose or aspartame loading. One subject reported slight nausea approximately 1.5 h after aspartame ingestion, but indicated that the symptoms were not those of a glutamate response. Plasma phenylalanine and aspartate levels were similar to those noted in normal subjects administered identical doses of aspartame. The data indicate no effect of aspartame loading in glutamate-susceptible subjects.
Pediatrics; VOL 93 ISS Jan 1994, P70-75, (REF 48)
IPA COPYRIGHT: ASHP To determine the effects of large doses of aspartame on behavior, cognition, and monoamine metabolism in children with attention deficit disorder, a randomized, double-blind, placebo-controlled crossover study was conducted in 15 children, ages 5-13 yr, with attention deficit disorder, who received aspartame 34 mg/kg or placebo every morning for alternate 2-wk periods. No clinically significant differences between aspartame and placebo were found for the various tests performed, including the Subjects Treatment Emergent Symptom Scale, Multigrade Inventory for Teachers, or Conners ratings, or for the Matching Familiar Figures Test or Airplane cognition tests.
Also, no differences were noted for any of the biochemical measures, except for the expected increase in plasma phenylalanine and tyrosine following aspartame. It was concluded that aspartame at greater than 10 times usual consumption has no effect on the cognitive and behavioral status of children with attention deficit disorder and does not appear to affect urinary excretion rates of monoamines and metabolites.
NEUROTOXICOLOGY (LITTLE ROCK); 10 (2). 1989. 229-238.
BIOSIS COPYRIGHT: BIOL ABS. These experiments examined the potential for single or repeated doses of aspartame to exacerbate or facilitate the production of seizures in Fischer-344 rats. In adult animals, 1,000 mg/kg of aspartame given by gavage acutely or over a 14 day period had no significant effect on the rate of kindling induced by stimulation of the prepyriform cortex.
A single dose of 1,000 mg/kg of aspartame had no effect on the number of animals developing tonic seizures after electroconvuslive shock, nor did aspartame affect the frequency or duration of seizure activity after pentylenetetrazol. In a second series of studies, young male and female rates were dosed with 1,000 mg/kg of aspartame on day 3-13 or 21-35 of age. Prior exposure to aspartame had no significant effect on the rate of kindling at 90 days of age. These experiments indicate that aspartame does not act a proconvulsant in rats.
EPILEPSIA; 36 (3). 1995. 270-275.
BIOSIS COPYRIGHT: BIOL ABS. The high intensity sweetener aspartame has been implicated anecdotally in seizure provocation. This possibility was investigated with a randomized, double-blind, placebo-controlled, cross-over study. After an extensive search, 18 individuals (16 adults and 2 children) who had seizures allegedly related to aspartame consumption were admitted to adult or pediatric epilepsy monitoring units where their EEG was monitored continuously for 5 days.
Aspartame (50 mg/kg) or identically enpackaged placebo was administered in divided doses at 0800, 1000, and 1200 h on study days 2 and 4. All meals were uniformly standardized on treatment days. No clinical seizures or other adverse experiences were observed after aspartame ingestion. Mean plasma phenylalanine (Phe) concentrations increased significantly after aspartame ingestion (83.6 muM) as compared with placebo (52.3 muM). Results suggest that aspartame, in acute dosage of 50 mg/kg, is no more likely than placebo to cause seizures.
Source: NEUROLOGY; 42 (5). 1992. 1000-1003.
BIOSIS COPYRIGHT: BIOL ABS. There are anecdotal reports of increased seizures in humans after ingestion of aspartame. We studied 10 children with newly diagnosed but untreated generalized absence seizures. Ambulatory cassette recording of EEG allowed quantification of numbers and length of spike-wave discharges in a double-blind study on two consecutive days. On one day the children received 40 mg/kg aspartame and on the other day, a sucrose-sweetened drink.
Baseline EEG was the same before aspartame and sucrose. Following aspartame compared with sucrose, the number of spike-wave discharges per hour and mean length of spike-wave discharges increased but not to a statistically significant degree. However, the total duration of spike-wave discharge per hour was significantly increased after aspartame (p=0.028), with a 40% | 17% (SEM) increase in the number of seconds per hour of EEG recording that the children spent in spike-wave discharge. Aspartame appears to exacerbate the amount of EEG spike wav
Source: Pediatrics; VOL 86 ISS Jul 1990, P75-83, (REF 43)
IPA COPYRIGHT: ASHP Two double-blind crossover design experiments were conducted in 20 healthy 9- to 10-yr-old children to evaluate the effect of aspartame (I) on learning, behavior and mood. In experiment one, the children received an ice slurry of strawberry Kool-Aid containing carbohydrate (polycose) plus either 34 mg/kg of I or the equivalent sweetness of cyclamate sodium. In experiment 2, the children received a drink of cold unsweetened strawberry Kool-Aid, containing 1.75 g/kg of sucrose (II) or 9.7 mg/kg of I.
Measures of associative learning, arithmetic calculation, activity level, social interaction, and mood were unaffected by treatment in experiment one. In experiment 2, the only significant treatment effect was on the frequency of minor and gross motor behaviors, which were less frequent after the consumption of II than after I. It was concluded that the effect of I appears to be related to its absence of metabolic consequences rather than to its amino acid composition and putative neurochemical impact.
Source: J. NUTR. 1983, 113(8):1600-1606
EIS: Epidemiology Information System BLOOD METHANOL CONCENTRATIONS WERE MEASURED IN 24 1-YEAR-OLD INFANTS ADMINISTERED ASPARTAME, A DIPEPTIDE METHYL ESTER SWEETENER. THE DOSES STUDIED INCLUDED A DOSE PROJECTED TO BE THE 99TH PERCENTILE OF DAILY INGESTION FOR ADULTS (34 MG BODY WEIGHT), A VERY HIGH USE DOSE (50 MG/KG BODY WEIGHT) AND A DOSE CONSIDERED TO BE IN THE ABUSE RANGE (100 MG/KG BODY WEIGHT). BLOOD METHANOL VALUES IN INFANTS WERE COMPARED TO VALUES OBSERVED PREVIOUSLY IN ADULTS ADMINISTERED EQUIVALENT DOSES OF ASPARTAME.
METHANOL CONCENTRATIONS WERE BELOW THE LEVEL OF DETECTION (0.35 MG/DL) IN THE BLOOD OF 10 INFANTS ADMINISTERED ASPARTAME AT 34 MG/KG BODY WEIGHT, BUT WERE SIGNIFICANTLY ELEVATED (P LESS THAN OR EQUAL TO 0.05) AFTER INGESTION OF ASPARTAME AT 50 AND 100 MG/KG BODY WEIGHT.
AT THE LATTER DOSES, MEAN PEAK BLOOD METHANOL CONCENTRATIONS AND THE AREA UNDER THE BLOOD METHANOL CONCENTRATION-TIME CURVE INCREASED IN PROPORTION TO DOSE. MEAN (+/- SEM) PEAK BLOOD METHANOL CONCENTRATION WAS 0.30 +/- 0.10 MG/100 ML AT A 50 MG/KG BODY WEIGHT ASPARTAME DOSE (N = 6) AND 1.02 +/- 0.28 MG/ML AT THE 100 MG/KG BODY WEIGHT DOSE (N = 8). BLOOD METHANOL VALUES IN INFANTS WERE SIMILAR TO THOSE OBSERVED IN NORMAL ADULTS./BLOOD
Ack! More caps! Again, I'm sorry.
Source: J TOXICOL ENVIRON HEALTH; 7 (2). 1981. 281-290.
HEEP COPYRIGHT: BIOL ABS. Blood methanol concentrations were measured in 30 normal adult subjects administered aspartame, a dipeptide methyl ester. The doses studied included the 99th percentile of projected daily ingestion (34 mg/kg body wt) and 3 doses considered to be in the abuse range (100, 150 and 200 mg/kg body wt). Methanol concentrations were below the level of detection (0.4 mg/dl) in the blood of the 12 normal subjects who ingested aspartame at 34 mg/kg. They were significantly elevated (P | 0.001) after ingestion of each abuse dose, with mean peak blood methanol concentrations and areas under the blood methanol concentration-time curve increasing in proportion to dose.
Mean (| SD) peak blood methanol concentrations were 1.27 | 0.48 mg/dl (100 mg/kg dose), 2.14 | 0.35 mg/dl (150 mg/kg dose) and 2.58 | 0.78 mg/dl at the (200 mg/kg dose). Blood methanol concentrations returned to predosing levels by 8 h after administration of the 100 mg/kg dose. Methanol was still detected in the blood 8 h after the subjects had ingested aspartame at 150 or 200 mg/kg. Blood formate analyses were carried out in 6 subjects who ingested aspartame at 200 mg/kg, since recent studies indicated that the toxic effects of methanol were due to formate accumulation.
No significant increase in blood formate concentrations over predosing concentrations was noted. No changes were noted in any blood chemistry profile parameters measured 24 h after aspartame ingestion, compared to values noted before administration. No differences were noted in ophthalmologic examinations carried out before and after aspartame loading.
Source: BRAIN RES; 520 (1-2). 1990. 351-353.
BIOSIS COPYRIGHT: BIOL ABS. Aspartame (L-aspartyl-L-phenylalanine methyl ester), an artificial low-calorie sweetner, was shown to dose-dependently inhibit L-(3H)glutamate binding to its N-methyl-D-aspartate-specific receptors. L-Aspartic acid, a major endogenous metabolite of aspartame, inhibited the binding more stronger than aspartame, while the other metabolites, L-phenylalanine and methanol, had no effect at the same concentration. Aspartame caused a significant change in the affinities of L-(3H)glutamate binding without altering the Vmax values of the binding, suggesting the inhibition is competitive. These in vitro findings suggested that aspartame may act directly on the N-methyl-D-asparate-sensitive glutamate recognition sites in the brain synaptic membranes.
Source: N. Engl. J. Med.; VOL 315 ISS Aug 14 1986, P456, (REF 10)
IPA COPYRIGHT: ASHP The case of a 31-yr-old woman who experienced migraines after heavy consumption of soft drinks and foods containing aspartame (NutraSweet; I) in doses of approximately 1000-5000 mg/day was reported. The onset of headaches normally occurred within one to 2 h after ingestion of 2-3 12 oz cans of soft drinks. During a 10-day trial of avoidance of all dietary soft drinks and added I, the patient noted a marked decrease, and then complete disappearance, of all headaches. Rechallenge with 500 mg of pure I in 14 oz of solution resulted in the occurrence of an identical headache within 1.5 h.
Source: Aviation, Space, and Environmental Medicine, Vol. 65, No. 1, pages 7-15, 28 references, 1994
The possible association of performance deficits on cognitive skills important in the cockpit and chronic ingestion of aspartame (22839470) was studied. In addition, the acute ethanol (64175) dosing element of an earlier study was replicated in the context of a modified and extended test battery, with particular concentration on the potential left frontal/right parietal deficits. The study subjects were university students. A counterbalanced, double blind, within subject design was adopted in which subjects took capsules for two 9 day periods completing both the aspartame and placebo conditions.
Each subject was tested using the SPARTANS cognitive test battery over four test sessions. No deleterious effects of aspartame on cognitive performance were recorded. The results showed a modest but statistically significant improvement in scores on three subtask variables which may or may not have been due to the aspartame. The outcome of the ethanol condition trials indicated that the current findings support those of earlier studies in most cases, with two areas of change. First, while the present findings replicate earlier studies for mean risk taking preference in that ethanol did not show any effect, it did not do so for risk taking consistency.
Present results also showed a significant effect of ethanol on memory search efficiency as indexed by the Sternberg task. Neither study indicated any significant effect on working memory, although short term memory problems are a classic symptom of chronic alcohol abuse.
That was only what I pulled from page 3 of 23... and I didn't pull all the results, only those I thought would be relevant. There's lots more information on aspartame, if you want to look for it!
August 19th, 2003, 10:41 AM
Oh Cripes! Could I get the Cliff Notes :DD ...g
August 19th, 2003, 11:58 AM
Oh Cripes! Could I get the Cliff Notes :DD ...g
ROFL!!!!! Exactly. :D :D
Actually, I will go back and read most of it when I've got more time. Thanks, Rachel!!
August 19th, 2003, 01:13 PM
Hee hee... I'll wait for you to read it and tell me what it says! I skimmed the titles of the abstracts, but that's it. :D
August 20th, 2003, 10:04 AM
Rache...thank you for all your input. I haven't had time to read thru it (I log on at work), but mainly skimmed thru it. Thank you for taking the time out!
August 20th, 2003, 10:16 AM
i skimmed through all of these. :rolleyes:
but one basic question in a language i understand - is it good or bad?
August 20th, 2003, 10:20 AM
You got me, smiles *shrugz*
August 20th, 2003, 10:54 AM
I'm waiting for Hollie to read it and tell me. :DD I can't think of much I use that contains aspartame, so it's not a huge concern for me right now... And I can pull up more results if anyone's interested. :twisted:
August 24th, 2003, 07:09 AM
I can speak from my own experience... Aspartame (the amount in one Diet Coke can) gave me headaches, and vertigo to the point where the room spun around me and I couldn't hold my head up. Embarrassing thing to happen in the middle of a meeting at work. :oops: ("No, sir, that really was just a Diet Coke, not a rum-and-Diet-Coke!")
Tying in with one of the abstracts mentioned above, I also get adverse effects from MSG (skin flushing and heart-racing), so I might be one of the type of people they mention.
MSM didn't do anything to me good or bad (short term; I don't take it now).
September 5th, 2003, 10:12 AM
I just skimmed through most of these, and the jist is no one can prove nothin'. (I spent four years of school doing nothing but skim abstracts about obscure experiments... brings back memories ::sigh::). They've done batteries of tests on these artificial sweeteners, and the only studies I know have that have shown any remotely conclusive evidence were done on saccharine (aka sweet n' low), and even then they were shown to slightly increase cancer risk in mice at dosages three to ten times higher than an average person can consume in one day.
In terms of anecdotal evidence, though, I've known a bunch of people to get headaches from the stuff, and we can't forget that when a truck of Diet Coke travels through Arizona (or anywhere else warm) the phenylanaline turns into Methane, which is, you know, poisonous and stuff :rolleyes: .
All that said, you'd have to pry my diet coke from my cold, dead hand before I'd give it up 8) :twisted:
September 5th, 2003, 10:32 AM
I noticed we almost have the same hair type (except my hair is fine and yours is medium)...do you have pictures of it wavy?
I did the experiment for T-Bear a few months ago and took pictures as my hair dried...you can see those at: